CHAMBERLAIN UNIVERSITY | ADVANCED PRACTICE NURSING PHARMACOLOGY
NR 566 Midterm Exam
Advanced Pharmacology
150 Questions and Answers — Verified
Latest Edition — A-Grade
Comprehensive coverage of all NR566 midterm domains:
Pharmacokinetics & Pharmacodynamics • Prescriptive Authority
Cardiovascular • Antimicrobial Stewardship • Endocrine/Diabetes
Respiratory • Pain Management • Integrated Case Studies
COGNITIVE LEVELS: 25% Recall | 55% Application | 20% Analysis
QUESTION DESIGN: 70% Scenario-Based | 25% Direct Recall | 5% Calculation
Aligned with 2026-2027 Chamberlain NR566 Curriculum Standards
Detailed rationales include pharmacokinetics, pharmacodynamics,
evidence-based guidelines, safety protocols, and clinical application
,NR 566 Midterm Exam — Advanced Pharmacology | 2026/2027 Verified 150 Questions | A-Grade Answers
NR 566 Midterm Exam — Instructions & Overview
This practice midterm examination contains exactly 150 multiple-choice questions designed to mirror the structure,
content domains, and cognitive complexity of the Chamberlain University NR 566 Advanced Pharmacology for Care of the
Family Midterm Examination. Every answer has been verified for clinical accuracy against the 2026-2027 Chamberlain
NR566 curriculum, current FDA prescribing labels, the 2026 American Diabetes Association Standards of Care, the GINA
2026 Global Strategy for Asthma Management and Prevention, the GOLD 2026 Report, the CDC Core Elements of
Outpatient Antibiotic Stewardship, the AGS Beers Criteria for Potentially Inappropriate Medication Use in Older Adults,
and DEA controlled substance scheduling.
The exam is divided into eight sections that progressively cover advanced pharmacokinetics and pharmacodynamics
(ADME, CYP450 system, drug interactions, half-life, therapeutic drug monitoring, and pharmacogenomics); legal/ethical
prescriptive authority (DEA regulations, controlled substances, PDMP, REMS, scope of practice); cardiovascular
pharmacology (antihypertensives, anticoagulants, antiplatelets, antidysrhythmics, heart failure, lipid management);
antimicrobial stewardship (antibiotics, antivirals, antifungals, resistance patterns, outpatient management); endocrine
and diabetes pharmacology (insulins, oral antidiabetics, GLP-1 agonists, SGLT2 inhibitors, thyroid agents, corticosteroids);
respiratory and asthma/COPD therapeutics (GINA/GOLD stepwise therapy); pain management and controlled substances
(opioids, NSAIDs, adjuvants); and comprehensive case studies requiring integration of multiple domains.
Each question provides four answer choices (A, B, C, D) with exactly one correct answer marked [CORRECT], followed by a
"Correct Answer" line and a detailed rationale explaining both why the correct answer is right and why the distractors are
wrong, citing pharmacokinetic principles, pharmacodynamic mechanisms, evidence-based guideline recommendations,
safety protocols, and clinical application. Approximately 70 percent of the questions are scenario-based (reflecting real
patient cases an advanced practice nurse encounters), 25 percent are direct recall of pharmacology facts and guideline
recommendations, and 5 percent involve calculations such as creatinine clearance, vancomycin dosing, and insulin
titration.
Students preparing for the NR566 midterm should aim for a minimum score of 85 percent on this practice test. Pay
particular attention to: warfarin target INR ranges (2.0-3.0 for AF/VTE vs. 2.5-3.5 for mechanical valves),
pregnancy-contraindicated medications (ACE inhibitors, ARBs, warfarin, isotretinoin, valproic acid), statin myopathy
monitoring, controlled substance schedules (Schedule II = no refills; III-V = up to 5 refills in 6 months), CYP450 inducers
(carbamazepine, phenytoin, rifampin, St. John's Wort) and inhibitors (ketoconazole, erythromycin, grapefruit juice,
cimetidine), insulin onset/peak/duration timing, beta-blocker cardioselectivity, SGLT2/GLP-1 cardiovascular and renal
benefits, metformin contraindications (eGFR <30), levothyroxine administration (empty stomach 30-60 min before food),
MRSA outpatient management (TMP-SMX, doxycycline), digoxin toxicity (potentiated by hypokalemia), and anticoagulant
reversal agents (vitamin K, protamine, idarucizumab, andexanet alfa). These are historically the most-missed items on
the NR566 midterm.
Section 1: Advanced Pharmacokinetics and Pharmacodynamics (ADME, CYP450
System, Drug Interactions, Half-Life, Therapeutic Drug Monitoring &
Pharmacogenomics) — Q1 to Q25
Q1: A 62-year-old female with epilepsy has been stable on carbamazepine for 3 years. She is newly prescribed
oral ketoconazole for a fungal infection. Three days later, she develops ataxia, nystagmus, and drowsiness.
Which pharmacokinetic mechanism best explains these findings?
A. Ketoconazole induces CYP3A4, increasing carbamazepine clearance and causing subtherapeutic levels.
Chamberlain University NR566 Curriculum Aligned Page 2 For Advanced Practice Nursing Preparation
,NR 566 Midterm Exam — Advanced Pharmacology | 2026/2027 Verified 150 Questions | A-Grade Answers
B. Ketoconazole is a potent CYP3A4 inhibitor, decreasing carbamazepine metabolism and causing carbamazepine
accumulation, toxicity (ataxia, nystagmus, drowsiness), and elevated serum levels. [CORRECT]
C. Ketoconazole displaces carbamazepine from plasma proteins, transiently increasing free drug levels only.
D. Ketoconazole accelerates renal excretion of carbamazepine, requiring a higher dose.
Correct Answer: B
Rationale: Ketoconazole is a potent inhibitor of CYP3A4, the primary enzyme responsible for carbamazepine metabolism.
Inhibition of CYP3A4 decreases carbamazepine clearance, leading to drug accumulation and dose-dependent toxicity (ataxia,
nystagmus, drowsiness, and potentially seizures paradoxically). Option A is wrong — ketoconazole is an inhibitor, not an
inducer (carbamazepine itself is the inducer). Option C describes protein-binding displacement, which is a transient effect that
does not cause sustained toxicity. Option D is wrong — ketoconazole does not accelerate carbamazepine renal excretion.
Q2: A patient asks why the provider recommended taking a particular medication with grapefruit juice as "it
might affect absorption." What is the actual mechanism by which grapefruit juice increases drug levels of certain
medications?
A. Grapefruit juice increases gastric acidity, enhancing drug absorption.
B. Grapefruit juice irreversibly inhibits intestinal CYP3A4 (and P-glycoprotein), reducing first-pass metabolism of
drugs such as felodipine, simvastatin, and cyclosporine, thereby increasing their oral bioavailability and serum
concentrations. [CORRECT]
C. Grapefruit juice alkalinizes the urine, slowing renal excretion of weak acids.
D. Grapefruit juice stimulates hepatic blood flow, increasing drug delivery to the liver.
Correct Answer: B
Rationale: Grapefruit juice irreversibly inhibits intestinal CYP3A4 and the efflux transporter P-glycoprotein (P-gp) in the gut
wall. This reduces first-pass metabolism of orally administered CYP3A4 substrates (e.g., felodipine, amlodipine, simvastatin,
lovastatin, cyclosporine, tacrolimus), significantly increasing their bioavailability and serum concentrations. The effect can last
up to 72 hours. Option A is wrong — grapefruit juice does not significantly alter gastric acidity. Option C is wrong — the effect is
at the intestinal wall, not the kidney. Option D is wrong — the mechanism is enzymatic inhibition in the gut, not increased
hepatic blood flow.
Q3: A 45-year-old male with HIV is started on abacavir. Two weeks later, he presents with fever, rash, nausea,
and shortness of breath that worsen rapidly. Which pharmacogenomic screening should have been performed
prior to initiating therapy, and what is the associated risk?
A. CYP2D6 genotyping; risk of poor metabolism.
B. HLA-B*5701 testing. Patients positive for HLA-B*5701 are at significantly increased risk of abacavir
hypersensitivity reaction, which can be fatal if the drug is rechallenged. Screening is recommended before
initiating abacavir. [CORRECT]
C. CYP2C19 genotyping; risk of immunologic non-response.
D. TPMT genotyping; risk of fatal myelosuppression.
Correct Answer: B
Rationale: HLA-B*5701 is a genetic marker strongly associated with abacavir hypersensitivity reaction (ABC HSR). Symptoms
include fever, rash, gastrointestinal symptoms, and respiratory symptoms that worsen with continued dosing. Rechallenge after
a hypersensitivity reaction can be fatal. HLA-B*5701 screening should be performed before initiating abacavir, and abacavir
should not be given to patients who test positive. Option A is wrong — CYP2D6 is not relevant to abacavir. Option C is wrong —
CYP2C19 affects clopidogrel, not abacavir. Option D is wrong — TPMT testing is for thiopurines (azathioprine,
6-mercaptopurine), not abacavir.
Chamberlain University NR566 Curriculum Aligned Page 3 For Advanced Practice Nursing Preparation
, NR 566 Midterm Exam — Advanced Pharmacology | 2026/2027 Verified 150 Questions | A-Grade Answers
Q4: A 58-year-old patient on warfarin with a target INR of 2.5 requires initiation of a new medication. Which of
the following genetic variations is most relevant to warfarin dosing sensitivity and bleeding risk?
A. CYP2D6 polymorphisms.
B. Variations in VKORC1 and CYP2C9. VKORC1 polymorphisms affect warfarin sensitivity (lower dose
requirements), while CYP2C9 polymorphisms (poor metabolizers) reduce warfarin clearance, both increasing
bleeding risk and necessitating lower initial dosing. [CORRECT]
C. HLA-B*1502.
D. CYP3A4 ultra-rapid metabolism.
Correct Answer: B
Rationale: VKORC1 (vitamin K epoxide reductase complex subunit 1) polymorphisms affect warfarin target sensitivity —
patients with the A/A genotype require significantly lower doses. CYP2C9 polymorphisms (CYP2C9*2 and *3 variants) reduce
warfarin clearance, prolonging half-life and increasing bleeding risk. Both genotypes should guide initial warfarin dosing per
FDA labeling and CPIC guidelines. Option A is wrong — CYP2D6 metabolizes codeine, tamoxifen, and many antidepressants, not
warfarin. Option C is wrong — HLA-B*1502 is associated with carbamazepine-induced Stevens-Johnson syndrome in Asian
populations. Option D is wrong — CYP3A4 is a minor pathway for warfarin metabolism (S-warfarin via CYP2C9; R-warfarin via
CYP1A2, CYP3A4).
Q5: A patient is described as a CYP2D6 ultra-rapid metabolizer. The provider plans to prescribe codeine for
postoperative pain. What is the clinical significance of this pharmacogenomic finding?
A. The patient will have no analgesic response to codeine.
B. CYP2D6 ultra-rapid metabolizers convert codeine to morphine more quickly and completely, leading to
potentially toxic morphine levels, respiratory depression, and fatal overdoses. Codeine should be avoided in
ultra-rapid metabolizers. [CORRECT]
C. The patient will require a higher codeine dose for analgesia.
D. Codeine will have an extended half-life in this patient.
Correct Answer: B
Rationale: Codeine is a prodrug that must be converted by CYP2D6 to morphine for analgesic effect. Ultra-rapid metabolizers
(multiple functional CYP2D6 gene copies) convert codeine to morphine more rapidly and completely, leading to potentially
toxic morphine levels, severe respiratory depression, and even fatal overdoses — particularly dangerous in breastfeeding
mothers (transmitting morphine to infants) and in children. Codeine (and tramadol) should be avoided in ultra-rapid
metabolizers. Option A describes poor metabolizers (no analgesia). Option C is wrong — ultra-rapid metabolizers would not
need higher doses (they would overdose). Option D is wrong — ultra-rapid metabolism means shorter, not extended, half-life.
Q6: A 67-year-old patient with atrial fibrillation has been on warfarin for 5 years with stable INRs between 2.0
and 3.0. She is newly prescribed rifampin for a tuberculosis exposure. What is the expected effect on her INR,
and what intervention is required?
A. INR will increase; warfarin dose should be decreased.
B. Rifampin is a potent CYP inducer that increases warfarin metabolism, causing the INR to decrease and
necessitating a significant warfarin dose increase (often 2-5 fold). Frequent INR monitoring is required during
rifampin use and for 1-2 weeks after discontinuation. [CORRECT]
C. INR will remain unchanged; no intervention needed.
D. Rifampin inhibits warfarin metabolism; switch to LMWH.
Correct Answer: B
Rationale: Rifampin is a potent inducer of hepatic CYP enzymes (particularly CYP2C9 and CYP3A4) that metabolize warfarin.
Induction increases warfarin clearance, lowering INR and increasing thrombotic risk. Significant warfarin dose increases (often
2-5 fold) are typically required to maintain therapeutic INR. Frequent INR monitoring is essential during rifampin therapy and
Chamberlain University NR566 Curriculum Aligned Page 4 For Advanced Practice Nursing Preparation
NR 566 Midterm Exam
Advanced Pharmacology
150 Questions and Answers — Verified
Latest Edition — A-Grade
Comprehensive coverage of all NR566 midterm domains:
Pharmacokinetics & Pharmacodynamics • Prescriptive Authority
Cardiovascular • Antimicrobial Stewardship • Endocrine/Diabetes
Respiratory • Pain Management • Integrated Case Studies
COGNITIVE LEVELS: 25% Recall | 55% Application | 20% Analysis
QUESTION DESIGN: 70% Scenario-Based | 25% Direct Recall | 5% Calculation
Aligned with 2026-2027 Chamberlain NR566 Curriculum Standards
Detailed rationales include pharmacokinetics, pharmacodynamics,
evidence-based guidelines, safety protocols, and clinical application
,NR 566 Midterm Exam — Advanced Pharmacology | 2026/2027 Verified 150 Questions | A-Grade Answers
NR 566 Midterm Exam — Instructions & Overview
This practice midterm examination contains exactly 150 multiple-choice questions designed to mirror the structure,
content domains, and cognitive complexity of the Chamberlain University NR 566 Advanced Pharmacology for Care of the
Family Midterm Examination. Every answer has been verified for clinical accuracy against the 2026-2027 Chamberlain
NR566 curriculum, current FDA prescribing labels, the 2026 American Diabetes Association Standards of Care, the GINA
2026 Global Strategy for Asthma Management and Prevention, the GOLD 2026 Report, the CDC Core Elements of
Outpatient Antibiotic Stewardship, the AGS Beers Criteria for Potentially Inappropriate Medication Use in Older Adults,
and DEA controlled substance scheduling.
The exam is divided into eight sections that progressively cover advanced pharmacokinetics and pharmacodynamics
(ADME, CYP450 system, drug interactions, half-life, therapeutic drug monitoring, and pharmacogenomics); legal/ethical
prescriptive authority (DEA regulations, controlled substances, PDMP, REMS, scope of practice); cardiovascular
pharmacology (antihypertensives, anticoagulants, antiplatelets, antidysrhythmics, heart failure, lipid management);
antimicrobial stewardship (antibiotics, antivirals, antifungals, resistance patterns, outpatient management); endocrine
and diabetes pharmacology (insulins, oral antidiabetics, GLP-1 agonists, SGLT2 inhibitors, thyroid agents, corticosteroids);
respiratory and asthma/COPD therapeutics (GINA/GOLD stepwise therapy); pain management and controlled substances
(opioids, NSAIDs, adjuvants); and comprehensive case studies requiring integration of multiple domains.
Each question provides four answer choices (A, B, C, D) with exactly one correct answer marked [CORRECT], followed by a
"Correct Answer" line and a detailed rationale explaining both why the correct answer is right and why the distractors are
wrong, citing pharmacokinetic principles, pharmacodynamic mechanisms, evidence-based guideline recommendations,
safety protocols, and clinical application. Approximately 70 percent of the questions are scenario-based (reflecting real
patient cases an advanced practice nurse encounters), 25 percent are direct recall of pharmacology facts and guideline
recommendations, and 5 percent involve calculations such as creatinine clearance, vancomycin dosing, and insulin
titration.
Students preparing for the NR566 midterm should aim for a minimum score of 85 percent on this practice test. Pay
particular attention to: warfarin target INR ranges (2.0-3.0 for AF/VTE vs. 2.5-3.5 for mechanical valves),
pregnancy-contraindicated medications (ACE inhibitors, ARBs, warfarin, isotretinoin, valproic acid), statin myopathy
monitoring, controlled substance schedules (Schedule II = no refills; III-V = up to 5 refills in 6 months), CYP450 inducers
(carbamazepine, phenytoin, rifampin, St. John's Wort) and inhibitors (ketoconazole, erythromycin, grapefruit juice,
cimetidine), insulin onset/peak/duration timing, beta-blocker cardioselectivity, SGLT2/GLP-1 cardiovascular and renal
benefits, metformin contraindications (eGFR <30), levothyroxine administration (empty stomach 30-60 min before food),
MRSA outpatient management (TMP-SMX, doxycycline), digoxin toxicity (potentiated by hypokalemia), and anticoagulant
reversal agents (vitamin K, protamine, idarucizumab, andexanet alfa). These are historically the most-missed items on
the NR566 midterm.
Section 1: Advanced Pharmacokinetics and Pharmacodynamics (ADME, CYP450
System, Drug Interactions, Half-Life, Therapeutic Drug Monitoring &
Pharmacogenomics) — Q1 to Q25
Q1: A 62-year-old female with epilepsy has been stable on carbamazepine for 3 years. She is newly prescribed
oral ketoconazole for a fungal infection. Three days later, she develops ataxia, nystagmus, and drowsiness.
Which pharmacokinetic mechanism best explains these findings?
A. Ketoconazole induces CYP3A4, increasing carbamazepine clearance and causing subtherapeutic levels.
Chamberlain University NR566 Curriculum Aligned Page 2 For Advanced Practice Nursing Preparation
,NR 566 Midterm Exam — Advanced Pharmacology | 2026/2027 Verified 150 Questions | A-Grade Answers
B. Ketoconazole is a potent CYP3A4 inhibitor, decreasing carbamazepine metabolism and causing carbamazepine
accumulation, toxicity (ataxia, nystagmus, drowsiness), and elevated serum levels. [CORRECT]
C. Ketoconazole displaces carbamazepine from plasma proteins, transiently increasing free drug levels only.
D. Ketoconazole accelerates renal excretion of carbamazepine, requiring a higher dose.
Correct Answer: B
Rationale: Ketoconazole is a potent inhibitor of CYP3A4, the primary enzyme responsible for carbamazepine metabolism.
Inhibition of CYP3A4 decreases carbamazepine clearance, leading to drug accumulation and dose-dependent toxicity (ataxia,
nystagmus, drowsiness, and potentially seizures paradoxically). Option A is wrong — ketoconazole is an inhibitor, not an
inducer (carbamazepine itself is the inducer). Option C describes protein-binding displacement, which is a transient effect that
does not cause sustained toxicity. Option D is wrong — ketoconazole does not accelerate carbamazepine renal excretion.
Q2: A patient asks why the provider recommended taking a particular medication with grapefruit juice as "it
might affect absorption." What is the actual mechanism by which grapefruit juice increases drug levels of certain
medications?
A. Grapefruit juice increases gastric acidity, enhancing drug absorption.
B. Grapefruit juice irreversibly inhibits intestinal CYP3A4 (and P-glycoprotein), reducing first-pass metabolism of
drugs such as felodipine, simvastatin, and cyclosporine, thereby increasing their oral bioavailability and serum
concentrations. [CORRECT]
C. Grapefruit juice alkalinizes the urine, slowing renal excretion of weak acids.
D. Grapefruit juice stimulates hepatic blood flow, increasing drug delivery to the liver.
Correct Answer: B
Rationale: Grapefruit juice irreversibly inhibits intestinal CYP3A4 and the efflux transporter P-glycoprotein (P-gp) in the gut
wall. This reduces first-pass metabolism of orally administered CYP3A4 substrates (e.g., felodipine, amlodipine, simvastatin,
lovastatin, cyclosporine, tacrolimus), significantly increasing their bioavailability and serum concentrations. The effect can last
up to 72 hours. Option A is wrong — grapefruit juice does not significantly alter gastric acidity. Option C is wrong — the effect is
at the intestinal wall, not the kidney. Option D is wrong — the mechanism is enzymatic inhibition in the gut, not increased
hepatic blood flow.
Q3: A 45-year-old male with HIV is started on abacavir. Two weeks later, he presents with fever, rash, nausea,
and shortness of breath that worsen rapidly. Which pharmacogenomic screening should have been performed
prior to initiating therapy, and what is the associated risk?
A. CYP2D6 genotyping; risk of poor metabolism.
B. HLA-B*5701 testing. Patients positive for HLA-B*5701 are at significantly increased risk of abacavir
hypersensitivity reaction, which can be fatal if the drug is rechallenged. Screening is recommended before
initiating abacavir. [CORRECT]
C. CYP2C19 genotyping; risk of immunologic non-response.
D. TPMT genotyping; risk of fatal myelosuppression.
Correct Answer: B
Rationale: HLA-B*5701 is a genetic marker strongly associated with abacavir hypersensitivity reaction (ABC HSR). Symptoms
include fever, rash, gastrointestinal symptoms, and respiratory symptoms that worsen with continued dosing. Rechallenge after
a hypersensitivity reaction can be fatal. HLA-B*5701 screening should be performed before initiating abacavir, and abacavir
should not be given to patients who test positive. Option A is wrong — CYP2D6 is not relevant to abacavir. Option C is wrong —
CYP2C19 affects clopidogrel, not abacavir. Option D is wrong — TPMT testing is for thiopurines (azathioprine,
6-mercaptopurine), not abacavir.
Chamberlain University NR566 Curriculum Aligned Page 3 For Advanced Practice Nursing Preparation
, NR 566 Midterm Exam — Advanced Pharmacology | 2026/2027 Verified 150 Questions | A-Grade Answers
Q4: A 58-year-old patient on warfarin with a target INR of 2.5 requires initiation of a new medication. Which of
the following genetic variations is most relevant to warfarin dosing sensitivity and bleeding risk?
A. CYP2D6 polymorphisms.
B. Variations in VKORC1 and CYP2C9. VKORC1 polymorphisms affect warfarin sensitivity (lower dose
requirements), while CYP2C9 polymorphisms (poor metabolizers) reduce warfarin clearance, both increasing
bleeding risk and necessitating lower initial dosing. [CORRECT]
C. HLA-B*1502.
D. CYP3A4 ultra-rapid metabolism.
Correct Answer: B
Rationale: VKORC1 (vitamin K epoxide reductase complex subunit 1) polymorphisms affect warfarin target sensitivity —
patients with the A/A genotype require significantly lower doses. CYP2C9 polymorphisms (CYP2C9*2 and *3 variants) reduce
warfarin clearance, prolonging half-life and increasing bleeding risk. Both genotypes should guide initial warfarin dosing per
FDA labeling and CPIC guidelines. Option A is wrong — CYP2D6 metabolizes codeine, tamoxifen, and many antidepressants, not
warfarin. Option C is wrong — HLA-B*1502 is associated with carbamazepine-induced Stevens-Johnson syndrome in Asian
populations. Option D is wrong — CYP3A4 is a minor pathway for warfarin metabolism (S-warfarin via CYP2C9; R-warfarin via
CYP1A2, CYP3A4).
Q5: A patient is described as a CYP2D6 ultra-rapid metabolizer. The provider plans to prescribe codeine for
postoperative pain. What is the clinical significance of this pharmacogenomic finding?
A. The patient will have no analgesic response to codeine.
B. CYP2D6 ultra-rapid metabolizers convert codeine to morphine more quickly and completely, leading to
potentially toxic morphine levels, respiratory depression, and fatal overdoses. Codeine should be avoided in
ultra-rapid metabolizers. [CORRECT]
C. The patient will require a higher codeine dose for analgesia.
D. Codeine will have an extended half-life in this patient.
Correct Answer: B
Rationale: Codeine is a prodrug that must be converted by CYP2D6 to morphine for analgesic effect. Ultra-rapid metabolizers
(multiple functional CYP2D6 gene copies) convert codeine to morphine more rapidly and completely, leading to potentially
toxic morphine levels, severe respiratory depression, and even fatal overdoses — particularly dangerous in breastfeeding
mothers (transmitting morphine to infants) and in children. Codeine (and tramadol) should be avoided in ultra-rapid
metabolizers. Option A describes poor metabolizers (no analgesia). Option C is wrong — ultra-rapid metabolizers would not
need higher doses (they would overdose). Option D is wrong — ultra-rapid metabolism means shorter, not extended, half-life.
Q6: A 67-year-old patient with atrial fibrillation has been on warfarin for 5 years with stable INRs between 2.0
and 3.0. She is newly prescribed rifampin for a tuberculosis exposure. What is the expected effect on her INR,
and what intervention is required?
A. INR will increase; warfarin dose should be decreased.
B. Rifampin is a potent CYP inducer that increases warfarin metabolism, causing the INR to decrease and
necessitating a significant warfarin dose increase (often 2-5 fold). Frequent INR monitoring is required during
rifampin use and for 1-2 weeks after discontinuation. [CORRECT]
C. INR will remain unchanged; no intervention needed.
D. Rifampin inhibits warfarin metabolism; switch to LMWH.
Correct Answer: B
Rationale: Rifampin is a potent inducer of hepatic CYP enzymes (particularly CYP2C9 and CYP3A4) that metabolize warfarin.
Induction increases warfarin clearance, lowering INR and increasing thrombotic risk. Significant warfarin dose increases (often
2-5 fold) are typically required to maintain therapeutic INR. Frequent INR monitoring is essential during rifampin therapy and
Chamberlain University NR566 Curriculum Aligned Page 4 For Advanced Practice Nursing Preparation
